CHAPTER XIII

ECLAMPSIA PARTURIENTIUM

The term Eclampsia was first used to describe the sudden exaltation,

flashing forth (_eklampsis_), of the vital faculties at puberty;

later it was applied to convulsions, but now it is restricted to

convulsions in pregnancy which sometimes begin suddenly, as in a

flash. The disease is characterized by a series of violent convulsive

movements, loss of consciousness, and coma, and is one of the most

dangerous complications of gestation. All convulsions and comas in

pregnancy, not due to hysteria, epilepsy, cervical tuberculosis,

apoplexy, pneumonia, phosphorus, strychnia and like poisons, uremia,

and meningitis, are commonly classed as eclamptic. When the symptoms

of eclampsia are present with the exception of the convulsions, a

rare condition, this state also is said to be eclampsia. Reineke[121]

reported a case like this. After death the heart, kidneys, and liver

showed all the signs of eclampsia.

[121] _Münchener medizinische Wochenschrift_, July 30, 1907.

The eclamptic attack may occur without warning, but almost always

there are premonitory symptoms for from a few hours to some weeks.

The preëclamptic symptoms are headache (commonly frontal), nausea

and vomiting, vertigo, nervous excitement or somnolence, muscle

twitching, occasional delirium, cramps in the calves, disturbances

of sight, tinnitus, and pain in the epigastrium. Epigastric pain,

headache, and disturbances of the optic tract are important symptoms.

If these last signs are present in a woman who has some edema and

nephritis, the eclampsia will certainly occur, if proper means to

relieve the condition are not promptly taken. When the prodromata

appear there is nephritis, as a rule, but exceptions are observed.

When the attack comes, if the patient is standing she falls

unconscious. The pupils dilate, the eyes and head are turned to

the side. She opens her mouth, and the jaw is pulled laterally.

The woman stiffens, her face is distorted, her arms bent, and the

whole body curves sidewise in a tonic spasm. After a few seconds her

jaws chop, and if her tongue is between the teeth it is lacerated;

twitching runs down from the face and ends in a violent convulsion

of the whole body, which may toss the patient from the bed, and she

may even fracture her skull or long bones in the fall. The breathing

stops, the bloodshot eyes stick out, the face swells and darkens, the

lips become purple. Gradually the convulsions wane, and the woman

appears to be dying; but after deep sighing she begins to breathe

stertorously; then she sinks into a coma, or, in favorable cases,

revives.

After a few minutes to an hour or more another convulsion may

befall her, or she may have no more than one. In very grave cases

consciousness may never return after the first fit. The convulsions

may run up into extraordinary numbers--a hundred or more. There is

a pseudoeclampsia where the convulsions have been as many as two

hundred. If there are many attacks in the first twenty-four hours

with no clear evidence of subsidence, the woman nearly always dies.

Fever begins in such cases, and goes up to 103 or even 107 degrees.

In an untreated case Black found a temperature of 110 degrees before

death. The average number of attacks in these cases is from five to

fifteen, and the convulsions are from a half minute to two or three

minutes apart. Olshausen had six patients who recovered after having

had from twenty-two to thirty-six convulsions, but those who have

above fifteen commonly die.

If the convulsions are severe the woman as a rule aborts, and often

rapidly. After the child is delivered the eclamptic symptoms may

subside, or they may come on again, even a week after labor. Often

the fetus dies during the attack; rarely it survives and is carried

to term; again, it may die and the eclampsia may subside, but the

fetus remains in the uterus for some time.

If the woman is to die the eclamptic attacks usually increase in

frequency and violence; the temperature runs up very high, or it

sinks; the pulse becomes weak and running, edema of the lungs comes

on, with rattling and cyanosis, and the urine ceases to flow. The

woman may die in a convulsion from apoplexy or heart paralysis. At

times the child is delivered, but the coma deepens and the woman

dies. In other cases there are coma and death without convulsions.

Rarely there is a condition akin to acute yellow atrophy of the

liver, with delirium, twitchings, coma, and death.

Women who have chronic nephritis seldom have convulsions in pregnancy

unless there happens to be cerebral hemorrhage as an effect, but

they suffer the other results of chronic Bright's disease--dropsy,

uremia, edema of the lungs, paralysis of the heart, and albuminuric

retinitis; they also are inclined to premature labor, and to

hemorrhages that loosen the placenta. When acute nephritis happens

in pregnancy convulsions are quite common, and when there are

convulsions as a result of either chronic or acute nephritis it is

very difficult to differentiate between these convulsions and genuine

eclampsia.

The real cause of eclampsia is unknown, but the most plausible

explanation of this "disease of theories," as Zweifel of Leipsic

called it, is that it is a toxemia which attacks the liver, and

directly or indirectly the kidneys, and brings on convulsions by

toxic action on the anterior cerebral cortex. The great difficulty is

to explain how these toxins originate. One authority suggests that

the poison comes from the liver; another, from the fetus; a third,

from the placenta, the intestines, the general metabolism, disturbed

glandular balance, bacteria, and so on, but nothing is certain as to

the etiology except that it is an intoxication.

On an average, 20 per cent. of the women who have eclampsia die,--but

statistics vary from 5.31 per cent. to 45.7 for the mother and from

30 to 42 per cent. for the child. Eclampsia occurring ante-partum

has the worst mortality; intra-partum, less; post-partum, least.

About half the children die from prematurity, toxemia, asphyxiation,

narcotics administered to the mother, or injuries at birth.

If the patient's pulse remains full and hard and below 120, there

is no immediate danger of death; but if faster, weaker, and running,

the prognosis is bad. High fever is not necessarily fatal to the

mother, but it is very dangerous to the fetus. Edema of the lungs is

a very grave symptom, but recovery is possible. When the convulsions

have gone beyond twenty the prognosis is bad, but there have been

recoveries. Deep cyanosis, marked restlessness, anuria, and intense

albuminuria are all bad symptoms. Apoplexy is nearly always fatal.

After delivery the recovery of the woman is by no means certain.

She may get pneumonia, sepsis, or another eclamptic attack. Hirst

finds that if the diastolic pressure does not rise above a ratio of

1 to 3 times the pulse pressure (_i. e._, the difference between the

systolic and diastolic pressures), the prognosis is good.

Every pregnant woman should be watched to prevent eclampsia, if

possible, because all are liable to this outcome. The hygienic

methods mentioned in the chapter on Abortion are most important here.

The family history is of weight--if the women of the patient's family

have been eclamptic, if her parents were alcoholic or insane, these

facts increase her liability to the disease. If she has had eclampsia

before, if her kidneys are acutely diseased,--especially if injured

by infections,--if she is inclined to digestive disturbance, she

is disposed to eclampsia. Albuminuria, diminishing amounts in the

daily excretion of urine, and decrease in the total solids of the

urine, casts or blood in the urine, are serious symptoms. If albumin

increases and urea decreases, this is a grave sign.

The blood should be examined for the various anemias. If the thyroid

gland is deficient or altered in activity, thyroid extract may be

indicated--this acts also as a diuretic. Uterine malpositions should

be corrected. Treatment should be given where there is any evidence

of toxemia, as headache, altered secretion and excretion, neuralgia,

mental eccentricity, increased vasomotor stimulation, high tension,

disturbance in the sensory apparatus, obstinate constipation and

jaundice. Toxemia is not necessarily renal in origin.

In any of these conditions the proteids should be kept low in the

diet, so that the kidneys may not be overtaxed. To throw off

toxins, the emunctories should be stimulated by laxatives, water

for diuresis, tepid bathing. If the symptoms grow threatening, and

the kidneys are involved, the woman should be put to bed, on water

alone. After three days an absolute milk diet should be begun. As she

improves, starches are added, then the vegetables containing proteid,

vegetable oils, and butter. As the improvement goes on, the diet may

be vegetables, fruit easy of digestion, and one egg a day. Later

fish and chicken are used, but never a full meat diet. Beef, mutton,

veal, and similar heavy meats are not to be eaten. The drink is to be

water, buttermilk, or koumiss.

When the eclampsia is inevitable the question of inducing labor

arises. If the child is not viable, abortion is out of the question,

as has been proved in the chapter on Abortion and the general chapter

on Homicide. If the child is viable, there are three opinions: one,

that the premature delivery should be effected as soon as possible;

a second, that this delivery should be delayed as long as possible;

and a third, that it should not be attempted at all. Those who hold

that the uterus should be emptied as soon as possible, induce labor

at the first convulsion, rapidly and under deep narcosis. Chloroform

is dangerous to the heart in such cases for full anesthesia; ether

is better. Braun first observed that the convulsions cease or are

lessened after delivery. Dührssen found these results in 93.72 per

cent., Olshausen in 85 per cent., Zweifel in 66 per cent. Peterson

said that in 615 cases of early delivery--as soon as possible after

the first convulsion--the maternal mortality was 15.9 per cent., but

28.9 per cent. in the same maternities under the expectant method.

Olshausen was not in favor of forced delivery. Charpentier[122]

held that forced delivery is dangerous and should be absolutely

proscribed. His statistics of mortality are: after spontaneous labor,

18.96; after artificial labor, 30.04; after forced delivery, 40.74.

[122] _Nouvelle Archives d'Obstétrique et de Gynécologie_, 1893.

Lichtenstein[123] reported, from Zweifel's clinic in Leipsic, the

results of 400 cases of eclampsia, and he found that the eclamptic

convulsions cease in only one-third of the cases after any form of

delivery. He says the mortality of induced labor is no better than

that after forced delivery, and that the mortality of both methods

does not materially differ from the mortality of a long series of

cases where there was no such intervention. The difference in the

mortality between eclampsia without delivery or with delivery seems

to depend on the relative loss of blood. In 40 per cent. of eclamptic

cases operated upon, the loss of blood was 500 c.c. above the loss

in cases of spontaneous delivery. The loss of blood tends to produce

collapse when the blood comes from the uterus, although it may be

beneficial if removed by venesection before delivery. Five hundred

c.c. of blood is one-eighth to one-ninth of the entire blood supply

of the body in a woman of average size. If 500 c.c. of blood is

withdrawn before the shock of forced delivery and replaced by an

equal quantity of normal salt solution, the toxin is thus reduced by

one-fourth or one-third and then diluted by the normal salt solution,

so that it has less poisonous effect.

[123] _Archiv für Gynäkologie_, 1911, xcv, 1.

Lichtenstein[124] describes the expectant treatment by phlebotomy

and narcotics to replace operative interference, and this method

has revolutionized the mortality of the treatment of eclampsia. In

ninety-four cases of eclampsia his mortality was only 5.3 per cent.,

and none of the deaths could be ascribed to the treatment. The

infant mortality was 37.3 per cent., as against his 38.8 per cent.

in active operative interference during preceding years. Werner, in

the Second Gynecological Clinic in the University of Vienna,[125] by

this new method in thirty-eight cases of eclampsia had a maternal

mortality of 5.2, as Lichtenstein had, but his infant mortality was

only 14.65 per cent., an enormous advance for the better. Formerly

the mortality in the Viennese clinic was 15.8 for the women and 44.3

for the children, in a series of 120 cases of eclampsia. A mortality

of 50 per cent. in the children is common in the old method. In

Lichtenstein's cases there were mental disturbances in 2.1 per cent.

of the women, as against 6.75 per cent. in the old method. Eclamptics

may go insane and kill the child after delivery. Lichtenstein treated

74 consecutive cases without a single death. In 54 per cent. of his

cases the convulsions ceased after one venesection, and 42 per cent.

of the women with ante-partum attacks recovered before labor came

on. Engelmann[126] reported a case where a woman who had had 188

convulsions recovered after the third venesection.

[124] _Monatsschrift für Geburtshülfe und Gynäkologie_, xxxviii,

2. Berlin.

[125] _Münchener medizinische Wochenschrift_, November 23, 1915.

[126] _Centralbl. f. Gynäk._ xxxi, 11.

In this method the woman is put in a dark, quiet room; 400 to 600

c.c. of blood are withdrawn by venesection, and 0.002 gm. morphine is

injected; two hours later 3 gm. chloral is given in an enema. If the

fetus presents in a position for prompt delivery it is removed with

forceps, or by expression to spare the mother; but expression is a

dangerous process always.

Zinke[127] of Cincinnati has a method which reduces the maternal

mortality, but it has an enormous infantile mortality. He depresses

the maternal pulse by veratrum viride, and this depression is

probably the cause of the infantile mortality through asphyxia. Veit

introduced the use of morphine in eclampsia, and Winckel the use of

chloral. It has been found that narcotics check the action of toxins

on the nuclei of cells, and in eclampsia the action of narcotics

may be of this nature. Baker of Alabama in 1859 first gave veratrum

viride in eclampsia. The drug lowers arterial tension by depressing

the vasomotor centres and the heart itself. In eclampsia it diverts

blood from the brain and depresses the motor neurons of the spinal

cord. Aconite has the same effect in acute cerebral congestion

without depressing the vasomotor centres or irritating the stomach as

veratrum viride does.

[127] _New York State Journal of Medicine_, xiii, 8.

Cesarean delivery is used frequently of late in eclampsia. The

mortality of the children is lowered somewhat by a cesarean section,

but the mortality of the mothers is much worse than in the expectant

method described by Lichtenstein. Eclamptic women usually have

badly affected kidneys, and the anesthetic used in the section may

be a cause of the raised mortality. Peterson reviewed 500 cases

of cesarean section for eclampsia[128] done by 259 operators in

various countries. Up to 1908 the maternal mortality was 47.97 per

cent. in 198 cases; from 1908 to 1913 it was 25.79 per cent. in

283 cases. Convulsions ceased in only 54.92 per cent. of the women

after cesarean delivery, and in those cases in which the convulsions

continued the mortality was 31.53 per cent. In 146 cases where the

convulsions ceased the mortality was still 19.8 per cent. for the

mothers. The fetal mortality was 10.69 per cent., counting all

children who died within three days after delivery by section. The

maternal mortality after cesarean section increases with the age of

the patient. The cesarean delivery, then, has a maternal mortality of

late of 25.79, with a tendency to increase as unskilled men attempt

it; the expectant method has a maternal mortality of only 5.3 per

cent. The cesarean delivery has a fetal mortality of 10.69 per cent.;

the expectant, 14.65 per cent. The expectant method is preferable.

[128] _Amer. Jour. Obstetrics and Diseases of Women and

Children_, lxix, 6.

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